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Article: Hyperdopaminergic status in experimental huntington disease

TitleHyperdopaminergic status in experimental huntington disease
Authors
KeywordsDopamine
Huntington disease
Chorea
Striatum
Substantia nigra pars compacta
Tyrosine hydroxylase
Ventral tegmental area
Issue Date2010
Citation
Journal of Neuropathology and Experimental Neurology, 2010, v. 69, n. 9, p. 910-917 How to Cite?
AbstractHuntington disease has been linked to increased dopaminergic neurotransmission in the striatum, and clinical studies have demonstrated that the associated chorea can be treated with dopamine antagonist or dopamine-depleting drugs. The origin of this hyperdopaminergic status is unknown. Because substantia nigra pars compacta and the ventral tegmental area are the main sources of striatal dopamine input, we hypothesized that changes in these regions relate to striatal dopaminergic alterations. Here, in a recently generated transgenic rat Huntington disease model that shows progressive striatal neurodegeneration and chorea, we found evidence ofincreased dopamine levels in the striatum. We also demonstrate more dopaminergic cells in the substantia nigra pars compacta and ventral tegmental area in these rats. These results suggest that increased striatal dopamine comes from these 2 main nuclei, and that it is not necessarily related to shrinkage of the striatum. The findings implicate increased dopamine input from these nuclei in the pathogenesis of chorea in Huntington disease. © 2010 by the American Association of Neuropathologists, Inc.
Persistent Identifierhttp://hdl.handle.net/10722/219862
ISSN
2015 Impact Factor: 3.432
2015 SCImago Journal Rankings: 2.136

 

DC FieldValueLanguage
dc.contributor.authorJahanshahi, Ali-
dc.contributor.authorVlamings, Rinske-
dc.contributor.authorKaya, Ahmet Hilmi-
dc.contributor.authorLim, Lee Wei-
dc.contributor.authorJanssen, Marcus L F-
dc.contributor.authorTan, Sonny-
dc.contributor.authorVisser-Vandewalle, Veerle-
dc.contributor.authorSteinbusch, Harry W M-
dc.contributor.authorTemel, Yasin-
dc.date.accessioned2015-09-24T04:44:09Z-
dc.date.available2015-09-24T04:44:09Z-
dc.date.issued2010-
dc.identifier.citationJournal of Neuropathology and Experimental Neurology, 2010, v. 69, n. 9, p. 910-917-
dc.identifier.issn0022-3069-
dc.identifier.urihttp://hdl.handle.net/10722/219862-
dc.description.abstractHuntington disease has been linked to increased dopaminergic neurotransmission in the striatum, and clinical studies have demonstrated that the associated chorea can be treated with dopamine antagonist or dopamine-depleting drugs. The origin of this hyperdopaminergic status is unknown. Because substantia nigra pars compacta and the ventral tegmental area are the main sources of striatal dopamine input, we hypothesized that changes in these regions relate to striatal dopaminergic alterations. Here, in a recently generated transgenic rat Huntington disease model that shows progressive striatal neurodegeneration and chorea, we found evidence ofincreased dopamine levels in the striatum. We also demonstrate more dopaminergic cells in the substantia nigra pars compacta and ventral tegmental area in these rats. These results suggest that increased striatal dopamine comes from these 2 main nuclei, and that it is not necessarily related to shrinkage of the striatum. The findings implicate increased dopamine input from these nuclei in the pathogenesis of chorea in Huntington disease. © 2010 by the American Association of Neuropathologists, Inc.-
dc.languageeng-
dc.relation.ispartofJournal of Neuropathology and Experimental Neurology-
dc.subjectDopamine-
dc.subjectHuntington disease-
dc.subjectChorea-
dc.subjectStriatum-
dc.subjectSubstantia nigra pars compacta-
dc.subjectTyrosine hydroxylase-
dc.subjectVentral tegmental area-
dc.titleHyperdopaminergic status in experimental huntington disease-
dc.typeArticle-
dc.description.natureLink_to_subscribed_fulltext-
dc.identifier.doi10.1097/NEN.0b013e3181ee005d-
dc.identifier.pmid20720506-
dc.identifier.scopuseid_2-s2.0-77957256940-
dc.identifier.volume69-
dc.identifier.issue9-
dc.identifier.spage910-
dc.identifier.epage917-

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